Aortic Regurgitation

 Incompetency of aortic valve leading to diastolic flow

of blood from aorta in to left ventricle.
 Causes
Acute Chronic
 Infective Endocarditis
 Dissecting Aorta
 Rupture of the Aortic leaflets
 Trauma
 Myxomatous valve
 Chronic
Congenital Acquired
 Bicuspid valve  RHD
 Aortpathy  Dilated Aorta
 Cystic medial necrosis  E.g HTN

 Collagen disorders  Degenerative

 E.g Marfan’s syndrome  Connective tissue disorders
 Ehler Denlos  E.g Ankylosing spondylitis
 Osteogenesis imperfecta  Rheumatoid arthritis

 Pseudoxanthoma elasticum  Reiter’s syndrome

 Giant cell artritis
 Syphilis
 Epidemiology
 AR is less common than AS
 Rheumatic heart disease is the most common cause of
AR throughout the world.
 In developed countries, congenital and degenerative
valve abnormalities are the most common cause and
the peak age of presentation is 40-60 years.
 Valvular causes are becoming less frequent and aortic
root causes now account for >50% of cases
Pathphysiology
Pathphysiology of Acute AR
Sudden volume overload on LV

LV unable to dilate acutely

LV end-diastolic pressure

Pulmonary venous pressure

Acute Pulmonary Edema

Pathphysiology of Chronic AR
Gradual volume overload on LV

LV is able to dilate

LVEDV without increase in end-diastolic pressure

Stroke volume

Eccentric hypertrophy and more dilatation

LV failure with increase in end-diastolic pressure

 Hemodynamics of AR

 Normal Condition  Severe acute AR

 Total SV increase
 Forward SV is reduced
 LVEDP rise
 Chronic compensated AR
 Increase EDV d/t eccentric hypertrophy
 Increase total and forward SV
 Volume overload is accommodated
 LV filling pressure is normalized
 ESV remains normal
 Chronic decompensated AR
 Impaired LV emptying
 Increase ESV
 Fall in EF, total and forward SV
 Further cardiac dilatation
 re-elevation of LV filling pressure
 Immediate after valve replacement
 EDV, ESV and filling pressure decreases
 Initially fall in EF
 Elimination of regurgitation
 Increase in forward stroke volume
 With time EF increases
What are the Stages of Chronic
aortic regurgitation???
Stage Defination Valve Valve Hemodynamic symptoms
anatomy hemodynamics consequences

A •At risk of AR •Congenital •AR severity •None •none

valve anomaly none or trace
•Disease of
aortic sinus or
ascending
aorta
•Aortic
sclerosis
•History of
Rheumatic
fever
•IE
Stage Defination Valve Valve Hemodynamic symptoms
anatomy hemodynamics consequences

B •Progressive •Mild to Mild AR: •Normal LV •none

AR Moderate •Jet width<25% of systolic function
calcification LVOT •Normal LV
of trileaflet •Vena contracta volume or mild
valve <0.3cm LV dilation
•Dilated •Rvol<30%
aortic sinuses •ERO<0.10cm2
•Rheumatic •Angiography
valve changes grade 1+
•Previous IE Mod AR:
•Jet width 25-64%
of LVOT
•Vena contracta
0.3-0.6cm
•Rvol 30-
59ml/beat
•RF30-49%
•ERO 0.10-0.29
cm2
•Angiography
grade 2+
Stage Defination Valve Valve Hemodynamic symptoms
anatomy hemodynamics consequences

C •Asymptomati •Calcific Severe AR: C1: •None

c Severe AR aortic valve •Jet width>65% •Normal LVEF •Exercise
disease of LVOT •Mild to mod LV testing is
•Congenital •Vena cntracta dilation reasnable to
anomoly >0.6 cm C2: confirm
•Dilated aortic •Holodiastolic •Abnormal LV symtoms
sinuses or flow reversal in systolic function status
ascending the proximal with depressed
aorta abd aorta LVEF or severe
•Rheumatic •Rvol>60ml/bea LV dilation
valve changes t
•IE with •RF 50%
abnormal •ERO>0.3 cm2
leaflet closure •Angiography
or perforation grade 3+ to 4+
•Severe AR
requires
evidence of LV
dilation
Stage Defination Valve Valve Hemodynamic symptoms
anatomy hemodynamics consequences

D •Symptomatic •Calcific aortic Severe AR: •Symptomatic •Extertional

severe AR valve disease •Jet width>65% severe AR may dyspnea
•Congenital of LVOT occur with •Angina
anomoly •Vena cntracta normal systolic •More severe
•Dilated aortic >0.6 cm function EF>50% HF symptoms
sinuses or •Holodiastolic Or
ascending flow reversal in •Mod LV
aorta the proximal dysfunction EF
•Rheumatic abd aorta 40-50%
valve changes •Rvol>60ml/ Or
•IE with •beat •Severe LV
abnormal •RF%50% dysfunction
leaflet closure •ERO>0.3 cm2 EF<40%
or perforation •Angiography •Moderate to
grade 3+ to 4+ sever LV dilation
•Severe AR present
requires
evidence of LV
dilation
 Symptoms
 Dyspnea
 Angina
 Symptoms of underlying cause
 Chest pain in Aortic Dissection
 Fever in infective Endocarditis
 Physical Examination
 There is very wide pulse pressure with assosiated signs:
 Water Hammer pulse: Big Volume, rise & collapses rapidly
 Corrigan’s Sign: Visible carotid pulsation
 De Musset’s sign: Head nodding with each pulse
 Muller’s sign: Visibel pulsation of uvula
 Traube’s sign: (Pistol shot femorals) Loud noise over femoral
 Quincke’s Sign: Visible capillary pulsation in the nail bed
 Duroziez Sign: Bruit in Femoral
 Hill’s Sign: Systolic BP in lower extremities>upper extremities
 >20 mmHg– Mild AR
 >40 mmHg– Moderate AR
 >60 mmHg– Severe AR
 Physical Examination
 Large amplitude, rapidly rising and rapidly collapsing

 Elevation of the arm accentuate the fast runoff of the

column of blood by gravity.
 Corrigan Sign
 De Musset’s Sign
 Quincke’s Sign
 Muller’s Sign
 Precordial Examination
 Inspection & Palpation

 Apex:
 Site: Displaced downward & laterally
 Character: Hyperdynamic
 Aortic Area:
 Aortic Pulsation
 Epigastric Area:
 Epigastric pulsation
  Auscultation:
 Sounds:
 A2 may be normal (or louder) if AR is due to aortic
root pathology

 It may be soft or absent if AR is due to aortic valve

pathology

 S3 may be heard with dilated LV

 Murmurs of AR:
 Site of maximal intensity: 3rd left intercostal space

 Site if main propagation: Apex

 Character: Soft, blowing decrescendo

 Timing: Early diastolic

 Relation to position: Best heard while the patient sitting up and

leaning forward in expiration.

 Duration of the murmur in diastole correlates with severity of

AR
 Austin Flint Murmur:
 Is a mid-diastolic murmur heared at the apex due to

elevation of anterior mitral leaflet by the regurgitant

blood from aorta causes relative MS

 Soft ejection systolic murmur:

 Due to increased blood flow across the aortic valve

(relative AS)
AHA guidelines for Dx of AR
 Recommendation COR LOE
TTE is indicated in patients with signs or I B
symptoms of AR (stages A to D) for accurate
diagnosis of the cause of regurgitation,
regurgitant severity, and LV size and systolic
function, and for determining clinical outcome
and timing of valve intervention

TTE is indicated in patients with dilated aortic I B

sinuses or ascending aorta or with a bicuspid
aortic valve (stages A and B) to evaluate the
presence and severity of AR
 Recommendation COR LOE
CMR is indicated in patients with moderate or I B
severe AR (stages B, C, and D) and suboptimal
echocardiographic images for the assessment
of LV systolic function, systolic and diastolic
volumes, and measurement of AR severity
 Diagnostic Testing
 ECG:
 Tachycardia
 Shows LVH with strain, left axis deviation
 New heart block may suggest an aortic root abscess
 CXR:
 Pulmonary edema
 Left ventricular enlargement and dilated aorta (Boot shaped
heart)
 Echocardiography:
TTE TEE
 LV systolic function  It clarifies better if TTE is
 LV dimensions at end systole unclear in following
and end diastole conditions
 Leaflet numbers and  Bicuspid valve
morphology  Aortic dissection

 Assessment of severity of AR  Endocarditis with root

abscess
 Look for evidence of
 Better visualization of aortic
endocarditis or aortic
valve in patient with a
dissection.
prosthetic valve
 Dimension of aortic root.
 MRI/CT:  Coronary Angiography:
 If Echo assesmnt of the  Who are undergoing
severity of AR is AVR and who are at risk
inadequate. for CAD
 CTA to evaluate  Assessment of LV
coronary anatomy prior pressure & LV function
to valvular surgery  To check severity if AR
in patients in whom it is
unclear on noninvasive
imaging
AHA guidelines of AR
Treatment
 Medical Therapy
Recommendation COR LOE
Treatment of hypertension (systolic BP >140 I B
mm Hg) is recommended in patients with
chronic AR (stages B and C), preferably with
dihydropyridine calcium channel blockers or
angiotensin-converting enzyme (ACE)
inhibitors/angiotensin-receptor blockers
(ARBs)

Medical therapy with ACE inhibitors/ARBs IIa B

and beta blockers is reasonable in patients
with severe AR who have symptoms and/or LV
dysfunction (stages C2 and D) when surgery is
not performed because of comorbidities
 Intervention
Recommendation COR LOE
AVR is indicated for symptomatic patients I B
with severe AR regardless of LV systolic
function
(stage D)

AVR is indicated for asymptomatic patients I B

with chronic severe AR and LV systolic
dysfunction (LVEF <50%) (stage C2)

AVR is indicated for patients with severe AR I C

(stage C or D) who are undergoing other
cardiac surgery
 Recommendation COR LOE
AVR is reasonable for asymptomatic patients IIa B
with severe AR with normal LV systolic
function (LVEF 50%), but severe LV dilation
(stage C2, LVESD >50 mm)

AVR is reasonable in patients with moderate IIa C

AR (stage B) who are undergoing other
cardiac surgery

AVR may be considered for asymptomatic IIb C

patients with severe AR and normal LV
systolic function (stage C1, LVEF ≥50%) but
severe LV dilation (LVEDD >65 mm) if
surgical risk is low
 Prognosis
 Chronic AR can be well tolerated for many years

 5 year survival is ~75% and 10 year survival is ~50%

 Prognosis worsen as symptoms develop

 Acute severe AR, is assosiated with high mortality

from LV failure and early surgical intervention is
indicated.
 Asymptomatic patients with normal LV function
 Progression to symptoms/signs of CHF <6%/year
 Progression to asymptomatic LV dysfunction <3.5%/year
 Sudden death <0.2%/year

 Asymptomatic patients with LV systolic dysfunction

 Progression to cardiac symptoms >25%/year

 Symptomatic patients
 Mortality rate >10%/year